Katoh K, Kaneko K, Nishiyama A
Pflugers Arch. 1986 Jan;406(1):1-5. doi: 10.1007/BF00582944.
The effect of the adrenergic neurotransmitter on K transport in the segments isolated from the rat submaxillary gland was investigated, employing the technique of electrical field stimulation (FS) and applying tyramine, a releasing drug for the catecholaminergic neurotransmitter. FS (16 Hz, 2 ms and 80 V for 1 min) caused a K release (peak value, 1.0 mumol/g/min) followed by a K uptake (peak value, 0.4 mumol/g/min) in the absence of any autonomic antagonist. Both FS-induced K release and uptake were blocked by the addition of tetrodotoxin (10(-7) g/ml). In the presence of atropine (1.4 X 10(-6) M), FS caused only a transient K uptake, which was abolished by the superimposed addition of propranolol (5 X 10(-6) M). Application of tyramine (6 X 10(-6)-6 X 10(-4) M) always only caused K uptake (peak value, 0.96 mumol/g/min), which was abolished by the addition of propranolol. The K uptake evoked either by FS or by tyramine application in the presence of atropine was not seen in the segments from rats pretreated (i.p.) with 6-hydroxydopamine. These results suggest that the adrenergic neurotransmitter activates mainly a beta-adrenergic receptor and evokes K uptake through receptor activation.
采用电场刺激（FS）技术并应用酪胺（一种儿茶酚胺能神经递质释放药物），研究了肾上腺素能神经递质对从大鼠下颌下腺分离的组织段中钾转运的影响。在没有任何自主神经拮抗剂的情况下，FS（16赫兹，2毫秒，80伏，持续1分钟）引起钾释放（峰值，1.0微摩尔/克/分钟），随后是钾摄取（峰值，0.4微摩尔/克/分钟）。添加河豚毒素（10^(-7)克/毫升）可阻断FS诱导的钾释放和摄取。在阿托品（1.4×10^(-6)摩尔/升）存在的情况下，FS仅引起短暂的钾摄取，叠加添加普萘洛尔（5×10^(-6)摩尔/升）可消除这种摄取。应用酪胺（6×10^(-6)-6×10^(-4)摩尔/升）总是仅引起钾摄取（峰值，0.96微摩尔/克/分钟），添加普萘洛尔可消除这种摄取。在用6-羟基多巴胺腹腔注射预处理的大鼠的组织段中，未观察到在阿托品存在的情况下由FS或酪胺应用引起的钾摄取。这些结果表明，肾上腺素能神经递质主要激活β-肾上腺素能受体，并通过受体激活引起钾摄取。
